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. Author manuscript; available in PMC: 2019 Feb 15.
Published in final edited form as: Adv Drug Deliv Rev. 2018 Jan 13;126:67–95. doi: 10.1016/j.addr.2018.01.008

Fig. 5.

Fig. 5

(A) Photomicrographs of retinal sections showing significant reduction in photoreceptor cell death in the murine model of human autosomal recessive retinitis pigmentosa, the rd10 mice at postnatal day (P) 18 after Adalimumab (ADA) treatment in comparison to control (C57Bl6) (TUNEL-stained sections revealing dead photoreceptors and PAR content in DAPI-counterstained sections); (B) Bar graph illustrating the effect of ADA on the number of TUNEL-positive nuclei and nuclear poly (ADP) ribose (PAR)-positive cells; (C) Photomicrographs of retinal sections showing reactive gliosis amelioration by ADA in the rd10 mouse retina at P18 (Iba1-labelling to visualize microglial cells and GFAP content in DAPI-counterstained sections); (D) Bar graphs illustrating the effect of ADA on migration index of microglia, the corrected fluorescence of GFAP content and TNFα gene expression; (E) Topical endoscopic fundal imaging (TEFI) images showing intravitreal administration of infliximab suppresses experimental autoimmune uveitis (EAU) in comparison to vehicle control; (F) combined total disease scores demonstrating the difference in clinical disease progression between treatment groups. In EAU control eyes typical disease progression with signs of raised optic disc, vasculitis and severe inflammation; In infliximab treated eyes, only raised optic disc and initial signs of vasculitis are evident; (G) Graph showing total CD45+ infiltrate numbers from individual eyes. Reprinted from [33, 34].